Department of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, United States.
Curr Pharm Des. 2019;25(18):2060-2070. doi: 10.2174/1381612825666190708155400.
Sepsis and septic shock are known to prompt multiple organ failure including cardiac contractile dysfunction, which is typically referred to as septic cardiomyopathy. Among various theories postulated for the etiology of septic cardiomyopathy, mitochondrial injury (both morphology and function) in the heart is perceived as the main culprit for reduced myocardial performance and ultimately heart failure in the face of sepsis.
Over the past decades, ample of experimental and clinical work have appeared, focusing on myocardial mitochondrial changes and related interventions in septic cardiomyopathy.
Here we will briefly summarize the recent experimental and clinical progress on myocardial mitochondrial morphology and function in sepsis, and discuss possible underlying mechanisms, as well as the contemporary interventional options.
众所周知,脓毒症和感染性休克会导致多器官衰竭,包括心肌收缩功能障碍,通常称为感染性心肌病。在提出的各种关于感染性心肌病病因的理论中,心脏中线粒体损伤(形态和功能)被认为是导致心肌功能降低以及面对脓毒症时最终发生心力衰竭的主要原因。
在过去的几十年中,已经出现了大量关于脓毒症性心肌病中线粒体变化及其相关干预的实验和临床工作。
在这里,我们将简要总结脓毒症中心肌线粒体形态和功能的最新实验和临床进展,并讨论可能的潜在机制以及当前的干预选择。